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To identify a high-sugar (HS) dietary pattern, a high-saturated-fat (HF) dietary pattern and a combined high-sugar and high-saturated-fat (HSHF) dietary pattern and to explore if these dietary patterns are associated with depressive symptoms.

Design

We used data from the HELIUS (Healthy Life in an Urban Setting) study and included 4969 individuals aged 18–70 years. Diet was assessed using four ethnic-specific FFQ. Dietary patterns were derived using reduced rank regression with mono- and disaccharides, saturated fat and total fat as response variables. The nine-item Patient Health Questionnaire (PHQ-9) was used to assess depressive symptoms by using continuous scores and depressed mood (identified using the cut-off point: PHQ-9 sum score ≥10).

Higher consumption of an HSHF dietary pattern is associated with more depressive symptoms and with depressed mood. Our findings reinforce the idea that the focus should be on dietary patterns that are high in both sugar and saturated fat.

There is increasing evidence for important roles of key cognitive processes, including attention, memory and learning, in the short-term decision making about eating. There is parallel evidence that people who are overweight or obese tend to perform worse on a variety of cognitive tasks. In this review, the evidence for these two ideas is summarised and then the idea that overconsumption of Western-style high-fat (HF)–high-sugar diets may underlie the association between obesity and poorer cognitive performance is explored. In particular, evidence in animals and human subjects that repeated consumption of HF or HF and sugar (HFS) diets leads to specific impairments in the functioning of the hippocampus, which underpin the consequent changes in cognition is summarised. These findings lead into the vicious cycle model (VCM), which suggests that these cognitive changes have knock-on negative effects for future appetite control, and evidence that altered hippocampal function is also associated with impaired appetite control is explored. The review concludes that there is consistent evidence in the animal literature and emerging evidence from human studies that supports this VCM. It is also noted, however, that to date studies lack the nutritional specificity needed to be able to translate these basic research findings into clear nutritional effects, and concludes that there is an urgent need for additional research to clarify the precise nature of the apparent effects of consuming HFS diets on cognition.

Palm oil is a cheap and versatile edible oil in widespread use as a food ingredient that has been linked to negative health and environmental outcomes. The current study aimed to understand the prospects for future health-focused policy development to limit food use of palm oil and promote a greater diversity of oils in Thailand’s food system.

Design

Eighteen semi-structured interviews were conducted with a range of stakeholders. The interviews probed views on the economic, health and environmental dimensions of the issue, the prospects for health-focused policy development and the policy development process. Transcripts were analysed using a health policy analytical framework.

Setting

Thailand.

Subjects

Stakeholders from a range of ministries, regulatory agencies, the private sector, non-governmental organizations and academia.

Results

There are several impediments to the emergence of strong regulation, including the primacy of economic considerations in setting policy, doubt and misperception about health implications and a complex regulatory environment with little space for health-related considerations. At the same time, some sections of the food industry producing food for domestic consumption are substituting palm with other oils on the basis of consumer health perceptions.

Conclusions

Strong regulation to curb the growth of palm oil is unlikely to emerge soon. However, a long-term strategy can be envisaged that relies on greater policy support for other indigenous oils, strategic rebalancing towards the use of palm oil for biofuels and oleochemicals, and harnessing Thailand’s food technology capabilities to promote substitution in food production in favour of oils with healthier fatty acid composition.

Eligible products (31 % of all Tick products in these categories) removed 4·1 million megajoules of energy, 156·0 tonnes of saturated fat, 15·4 tonnes of trans-fat and 4·0 tonnes of sodium from food products sold in New Zealand over three years. In each food category, these Tick products were, on average, 14–76 % lower in energy, saturated fat, trans-fat and sodium than non-Tick products, indicating healthier options. Participating manufacturers reported that international market trends and consumer demand for tasty, healthy foods primarily influenced Tick product development and sales. Tick was used as part of their marketing strategy as it was perceived as a credible, well-recognised logo for New Zealand consumers. Tick was cited as the primary initiative encouraging saturated fat reduction.

Conclusions

The Tick Programme is continuing to encourage manufacturers to make meaningful improvements to the nutritional quality of the New Zealand food supply. Over time, these changes are likely to influence population nutrient intakes and reduce CVD risk factors.

Coconut, Cocos nucifera L., is a tree that is cultivated to provide a large number of products, although it is mainly grown for its nutritional and medicinal values. Coconut oil, derived from the coconut fruit, has been recognised historically as containing high levels of saturated fat; however, closer scrutiny suggests that coconut should be regarded more favourably. Unlike most other dietary fats that are high in long-chain fatty acids, coconut oil comprises medium-chain fatty acids (MCFA). MCFA are unique in that they are easily absorbed and metabolised by the liver, and can be converted to ketones. Ketone bodies are an important alternative energy source in the brain, and may be beneficial to people developing or already with memory impairment, as in Alzheimer's disease (AD). Coconut is classified as a highly nutritious ‘functional food’. It is rich in dietary fibre, vitamins and minerals; however, notably, evidence is mounting to support the concept that coconut may be beneficial in the treatment of obesity, dyslipidaemia, elevated LDL, insulin resistance and hypertension – these are the risk factors for CVD and type 2 diabetes, and also for AD. In addition, phenolic compounds and hormones (cytokinins) found in coconut may assist in preventing the aggregation of amyloid-β peptide, potentially inhibiting a key step in the pathogenesis of AD. The purpose of the present review was to explore the literature related to coconut, outlining the known mechanistic physiology, and to discuss the potential role of coconut supplementation as a therapeutic option in the prevention and management of AD.

Fast foods are often energy dense and offered in large serving sizes. Observational data have linked the consumption of fast foods to an increased risk of obesity and related diseases.

Design

We surveyed the reported energy, total fat and saturated fat contents, and serving sizes, of fast-food items from five major chains across ten countries, comparing product categories as well as specific food items available in most countries.

Setting

MRC Human Nutrition Research, Cambridge, UK.

Subjects

Data for 2961 food and drink products were collected, with most from Canada (n 550) and fewest from the United Arab Emirates (n 106).

Results

There was considerable variability in energy and fat contents of fast foods across countries, reflecting both the portfolio of products and serving size variability. Differences in total energy between countries were particularly noted for chicken dishes (649–1197 kJ/100 g) and sandwiches (552–1050 kJ/100g). When comparing the same product between countries variations were consistently observed in total energy and fat contents (g/100 g); for example, extreme variation in McDonald’s Chicken McNuggets with 12 g total fat/100 g in Germany compared with 21·1 g/100 g in New Zealand.

Conclusions

These cross-country variations highlight the possibility for further product reformulation in many countries to reduce nutrients of concern and improve the nutritional profiles of fast-food products around the world. Standardisation of serving sizes towards the lower end of the range would also help to reduce the risk of overconsumption.

Lutein and zeaxanthin are xanthophyll carotenoids present in highly pigmented vegetables and fruits. Lutein is selectively accumulated in the brain relative to other carotenoids. Recent evidence has linked lutein to cognition in older adults, but little is known about lutein in young children, despite structural brain development. We determined lutein intake using FFQ, one 24 h recall and three 24 h recalls, plasma lutein concentrations and their association with cognition in 160 children 5·6–5·9 years of age, at low risk for neurodevelopmental delay. Plasma lutein was skewed, with a median of 0·23 (2·5th to 95th percentile range 0·11–0·53) µmol/l. Plasma lutein showed a higher correlation with lutein intake estimated as the average of three 24 h recalls (r 0·479; P = 0·001), rather than one 24 h recall (r 0·242; P = 0·003) or FFQ (r 0·316; P = 0·001). The median lutein intake was 697 (2·5th to 95th percentile range 178–5287) µg/d based on three 24 h recalls. Lutein intake was inversely associated with SFA intake, but dietary fat or SFA intakes were not associated with plasma lutein. No associations were found between plasma lutein or lutein intake and any measure of cognition. While subtle independent effects of lutein on child cognition are possible, separating these effects from covariates making an impact on both child diet and cognition may be difficult.

Non-alcoholic fatty liver disease is associated with insulin resistance and dyslipidaemia and can progress to steatohepatitis and cirrhosis. We sought to determine whether dietary fat and saturated fat content alter liver fat in the absence of weight change in an older population. Liver fat was quantified by magnetic resonance spectroscopy before and after 4 weeks on an isoenergetic low-fat/low-saturated fat/low-glycaemic index (LGI) (LSAT: 23 % fat/7 % saturated fat/GI < 55) or a high-fat/high-saturated fat/high-GI (HSAT: 43 % fat/24 % saturated fat/GI>70) diet in older subjects. In the present study, twenty subjects (seven males/thirteen females; age 69·3 (sem 1·6) years, BMI 26·9 (sem 0·8) kg/m2) were randomised to the LSAT diet and fifteen subjects (six males/nine females; age 68·6 (sem 1·8) years, BMI 28·1 (sem 0·9) kg/m2) to the HSAT diet. Weight remained stable. Liver fat decreased significantly on the LSAT diet (median 2·2 (interquartile range (IQR) 3·1) to 1·7 (IQR 1·8) %, P= 0·002) but did not change on the HSAT diet (median 1·2 (IQR 4·1) to 1·6 (IQR 3·9) %). The LSAT diet lowered fasting glucose and total cholesterol, HDL-cholesterol and LDL-cholesterol and raised TAG (P< 0·05), while the HSAT diet had no effect on glucose or HDL-cholesterol but increased total cholesterol and LDL-cholesterol (P< 0·05). Fasting insulin and homeostasis model of insulin resistance did not change significantly on either diet, but the Matsuda index of insulin sensitivity improved on the LSAT diet (P< 0·05). Assignment to the LSAT v. HSAT diet was a predictor of changes in lipid parameters but not liver fat. We conclude that diet composition may be an important factor in the accumulation of liver fat, with a low-fat/low-saturated fat/LGI diet being beneficial.

The Inuit population is often described as being protected against CVD due to their traditional dietary patterns and their unique genetic background. The objective of the present study was to examine gene–diet interaction effects on plasma lipid levels in the Inuit population. Data from the Qanuippitaa Nunavik Health Survey (n 553) were analysed via regression models which included the following: genotypes for thirty-five known polymorphisms (SNP) from twenty genes related to lipid metabolism; dietary fat intake including total fat (TotFat) and saturated fat (SatFat) estimated from a FFQ; plasma lipid levels, namely total cholesterol (TC), LDL-cholesterol (LDL-C), HDL-cholesterol (HDL-C) and TAG. The results demonstrate that allele frequencies were different in the Inuit population compared with the Caucasian population. Further, seven SNP (APOA1 − 75G/A (rs670), APOB XbAI (rs693), AGT M235T (rs699), LIPC 480C/T (rs1800588), APOA1 84T/C (rs5070), PPARG2 − 618C/G (rs10865710) and APOE 219G/T (rs405509)) in interaction with TotFat and SatFat were significantly associated with one or two plasma lipid parameters. Another four SNP (APOC3 3238C>G (rs5128), CETP I405V (rs5882), CYP1A1 A4889G (rs1048943) and ABCA1 Arg219Lys (rs2230806)) in interaction with either TotFat or SatFat intake were significantly associated with one plasma lipid variable. Further, an additive effect of these SNP in interaction with TotFat or SatFat intake was significantly associated with higher TC, LDL-C or TAG levels, as well as with lower HDL-C levels. In conclusion, the present study supports the notion that gene–diet interactions play an important role in modifying plasma lipid levels in the Inuit population.

Foods high in monounsaturated fat, such as olive oil, and endurance exercise are both known to independently reduce postprandial TAG concentrations. We examined the combined effects of exercise and dietary fat composition on postprandial TAG concentrations in nine healthy pre-menopausal females (age 26·8 (sd 3·3) years, BMI 22·3 (sd 2·0) kg/m2). Each participant completed four, 2 d trials in a randomised order: (1) butter–no exercise, (2) olive oil–no exercise, (3) butter–exercise, (4) olive oil–exercise. On day 1 of the exercise trials, participants walked or ran on a treadmill for 60 min. On the no-exercise trials, participants rested on day 1. On day 2 of each trial, participants rested and consumed an olive oil meal (saturated fat 15 % and unsaturated fat 85 %) or a butter meal (saturated fat 71 % and unsaturated fat 29 %) for breakfast. Venous blood samples were obtained in the fasted state and for 6 h postprandially on day 2. A significant main effect on physical activity (exercise or control) was obtained for plasma TAG concentration (three-way ANOVA, P = 0·043), and the total area under the concentration v. time curve for TAG was 26 % lower on the olive oil–exercise trial (4·40 (sd 0·40) mmol × 6 h/l) than the butter–no exercise trial (5·91 (sd 1·01) mmol × 6 h/l) (one-way ANOVA, P = 0·029). These findings suggest that the combination of exercise and a preference for monounsaturated dietary fat intake in the form of olive oil may be most beneficial for reducing postprandial TAG concentrations.

A recent meta-analysis of prospective cohort studies has not found an association between dietary saturated fat intake and CHD incidence. This funnelled the discussion about the importance of the recommendation to lower the intake of saturated fat for the prevention of CHD. At the same time a document of the European Food Safety Authority has suggested that specific quantitative recommendations are not needed for individual fatty acids but that more general statements can suffice. In this review, we discuss methodological aspects of the absence of association between SFA intake and CHD incidence in prospective cohort studies. We also summarise the results of the controlled dietary experiments on blood lipids and on CHD incidence in which saturated fat was replaced by either cis-unsaturated fat or carbohydrates. Finally, we propose a nutritionally adequate diet with an optimal fatty acid composition for the prevention of CHD in the context of dietary patterns. Such diets are characterised by a low intake of saturated fat, and as low as possible intake of trans-fat and fulfil the requirements for the intake of n-6 and n-3 fatty acids. No recommendation is needed for the intake of cis-MUFA.

The objective of the present study was to compare the acute effect of meals of different composition on the expression of adhesion molecules that play a key role in leucocyte trafficking. A total of twenty apparently healthy subjects randomly consumed three isoenergetic meals 1 week apart: enriched in carbohydrates (CHO), enriched in monounsaturated fat and enriched in saturated fat. Blood samples were obtained before the meals and at 2, 4, 6, 8 and 10 h after meal ingestion. Samples were analysed for LDL resistance to Cu-mediated oxidation and for the surface expression on peripheral blood mononuclear cells (PBMC) of CD62L, CD162, CD11a, CD11b, CD49d and CD54 by flow cytometry. The present results showed that there were no changes in LDL susceptibility to oxidation within and among the meals. After the CHO-enriched meal, there was a time-dependent increased expression of CD162, CD49d, CD11a and CD54 on PBMC that returned to basal values after 8–10 h. These changes were significantly greater than the ones observed after the consumption of the monounsaturated fat- and the saturated fat-enriched meals and were more evident in lymphocytes than in monocytes. In conclusion, acute ingestion of a CHO-enriched meal induces higher increases of lymphocyte activation markers than fat-enriched meals. These results suggest that long-term consumption of CHO-enriched diets may be associated with a sustained pro-inflammatory state.

Dietary fatty acids (FA) are the major determinants of blood lipids, and measurements of plasma phospholipid FA (PL-FA) composition that reflect the dietary intake of FA may provide insights into the relationships between diet and CHD. We assessed CHD mortality associations with PL-FA (SFA, PUFA and MUFA) levels measured in a nested case–control study of 116 cases of CHD death and 239 controls that were frequency-matched for age and employment grade. The participants had plasma levels of total cholesterol, LDL-cholesterol (LDL-C), HDL-cholesterol, apo B and apo A1, C-reactive protein (CRP) and fibrinogen recorded. SFA levels were significantly positively correlated with total cholesterol, LDL-C, apo B, CRP protein and fibrinogen. By contrast, phospholipid-PUFA were inversely associated with CRP, but not with any of the lipids. A higher SFA content (top v. bottom quarter) was associated with a 2-fold higher risk of CHD (OR and 95 % CI: OR 2·12; 95 % CI: 1·13, 3·99), and an equivalent difference in PUFA was associated with a halving in CHD risk (OR 0·49; 95 % CI: 0·26, 0·94), but MUFA was unrelated to CHD risk. These associations were substantially attenuated, after additional adjustment for lipids and inflammatory markers. Higher levels of saturated fat and lower levels of polyunsaturated fats were each associated with a higher risk of CHD in elderly men, and these associations were partly explained by their effects on blood lipids and biomarkers of inflammation.

The aim of the present study was to examine the effect of reducing saturated fat in the diet, or partly replacing it with unsaturated fat, on the serum lipoprotein profile of human subjects. The study had two intervention periods, 8 weeks (phase 1) and 52 weeks (phase 2). In phase 1, total fat was reduced from 31 to 25 % energy (polyunsaturated fatty acids (PUFA):saturated fatty acids (SFA) ratio increased from 0.2 to 0.4) by reducing the quantity of coconut fat (CF) in the diet from 17.8 to 9.3 % energy intake. In phase 2, subjects were randomised to groups A and B. In group A total fat was reduced from 25 to 20 % energy (PUFA:SFA ratio increased from 0.4 to 0.7) by reducing the quantity of CF in the diet from 9.3 to 4.7 % total energy intake. In group B, the saturated fat content in the diet was similar to group A. In addition a test fat (a mixture of soyabean oil and sesame oil, PUFA:monosaturated fatty acids ratio 2) contributed 3.3 % total energy intake and total fat contributed 24 % energy intake (PUFA:SFA ratio increased from 0.7 to 1.1). At the end of phase 1, there was a 7.7 % reduction in cholesterol (95 % CI -3.6, -12.2) and 10.8 % reduction in LDL (95 % CI -4.9, -16.5) and no significant change in HDL and triacylglycerol. At the end of phase 2, the reduction in cholesterol in both groups was only about 4 % (95 % CI -12, 3.2) partly due the concomitant rise in HDL. The reduction in LDL at 52 weeks was significantly higher in group B (group A mean reduction 11 %, 95 % CI -20.1, -2.0 and group B mean reduction 16.2 % 95 % CI -23.5, -8.9). In phase 2, triacylglycerol levels showed a mean reduction of 6.5 % in group 2A and a mean increase of 8.2 % in group 2B. The reduction of saturated fat in the diet is associated with a lipoprotein profile that would be expected to reduce cardiovascular risk. The reduction of dietary saturated fat with partial replacement of unsaturated fat brings about changes in total cholesterol, HDL- and LDL-cholesterol that are associated with a lower cardiovascular risk.

Expert scientific advice to the UK Government has been translated into eight general dietary guidelines, which form the core of population-based dietary advice in the UK and are supplemented by a food selection guide showing the types and proportions of foods needed for a balanced and healthy diet. Data from the Dietary and Nutritional Survey of British Adults were used to identify statistically significant differences between subgroups of the study population that met, or failed to meet, population nutritional goals for intakes of total fat, saturated fat and dietary fibre. Several eating habits — including greater consumption of starchy foods (particularly wholemeal varieties), greater consumption of fruit and the substitution of reduced-fat milk for whole-fat milk — were shared by the subgroups that met each of the nutritional goals. This analysis provides clues for any future refinement of food-based dietary guidelines.

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